Meerson F Z, Kagan V E, Belkina L M
Basic Res Cardiol. 1982 Sep-Oct;77(5):465-85. doi: 10.1007/BF01907940.
A working hypothesis on pathogenesis of ischemic heart damage has been proposed. According to this hypothesis, a crucial role in conversion of reversible damage into irreversible damage is played by cardiomyocyte membrane destruction caused by the so-called "lipid triad". The latter comprises activation of lipid peroxidation, activation of phospholipases, and the detergentlike action of excessive amounts of free fatty acids and lysophospholipids. Marked activation of lipid peroxidation in experimental myocardial infarction, as well as reoxygenation following transitory ischemia, have been demonstrated. The proposed hypothesis and experimental data underly successful application of synthetic free radical scavengers (antioxidants) for heart protection against experimental myocardial infarction, transitory ischemia, and emotional, painful stress.
关于缺血性心脏损伤发病机制的一个工作假说已经提出。根据这一假说,所谓的“脂质三联征”导致的心肌细胞膜破坏在可逆性损伤转变为不可逆性损伤过程中起关键作用。脂质三联征包括脂质过氧化激活、磷脂酶激活以及过量游离脂肪酸和溶血磷脂的去污剂样作用。实验性心肌梗死以及短暂性缺血后的再灌注过程中脂质过氧化的显著激活已得到证实。所提出的假说和实验数据为合成自由基清除剂(抗氧化剂)成功用于保护心脏免受实验性心肌梗死、短暂性缺血以及情绪性、疼痛性应激的影响奠定了基础。